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Acute Renal Failure for the Intern
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Background and Epidemiology
Affects 5%-7% of all hospitalized patients
20%-70% mortality rate overall
ARF in ICU – 50%-70% mortality rate
Mortality rate unchanged over past 50 years
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Anatomy 1
Renal Arteries
Kidneys
Glomerulus
Collecting system
Ureter
Bladder
Urethra
Renal Vein
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Anatomy 2
Glomerulus
PCT
Loop of Henle
DCT
Collecting system
130 to 180 liters is filtered across the glomerulus every day. 98 to 99 % of that filtrate is reabsorbed.
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Estimations of Renal Function
What do the kidneys do?
How can we measure the function of the kidneys?
What is the “ideal” substance to measure?
What do we commonly use to measure renal function?
Filter the blood
Measure the glomeular filtration of a substance within the kidneys
•Completely filtered
•Not secreted
•Not reabsorbed / transported
Serum Creatinine Concentration
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Creatinine
Water soluble breakdown product of creatine from skeletal muscle (and ingested meat, suplements).
Creatinine is released into the circulation at a relatively constant rate.
Creatinine is freely filtered in the glomerulus, and is not metabolized by the kidney.
Approximately 15% of the urinary creatinine is secreted in the proximal tubule (in normally functioning kidney).
Remember: Not all individuals will
have the same amount of creatinine in their blood.
Different drugs can affect the concentration of serum creatinine (without affecting a patient’s renal function).
Cimetidine Trimethoprim
Decrease Creatinine Secretion Rise in serum level by up to 0.5 mg/dl
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Effects on Serum Creatinine
Decreased Creatinine Secretion Cimetidine >> Ranitidine & Famotidine Trimethoprim
Interfere with the Assay Acetoacetate (Diabetic Ketoacidosis) Cefoxitin Flucytosine
Enhanced Creatinine Production Large meat meal Creatine containing supplements Rhabdomyolysis
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Serum Creatinine and Renal Function
Glomerular Filtration Rate Cockcroft-Gault Method Jelliffe Method MDRD
(140 – age) * weight (kg)
72 * serum Creatinine
(multiply by 0.85 for female)
[98 – 0.8 * (age – 20)] * BSA
1.73 * serum Creatinine
(multiply by 0.9 for female)
186 * sCr ^ (-1.154) * Age ^ (-0.203)
Multiple by 0.743 for female
Multiply by 1.21 for African American
•Assumes albumin = 4.0
•Assumes patient is ~ 1.73 m2
95 +/- 20 ml/min in women
120 +/- 25 ml/min in men
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Which formula should you use?
Strengths & Weaknesses MDRD
Underestimates patients with normal renal function
Overestimates patients with severe renal impairment.
Cockcroft-Gault Underestimates patients at older ages Overestimates patients at younger ages
All of these formulas are best used in patient’s with stable renal function. It takes time for the serum
creatinine level to accurately reflect renal function.
We usually use the Modification of Diet in Renal Disease (MDRD) forumula. Levey et al. Ann Intern Med.
Mar 1999.
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What is Acute Renal Failure?
Increase in sCr > 0.5 mg/dl (44 umol/l)
Increase in sCr > 2-fold
Decrease in GFR > 50%
Decrease in GFR requiring dialysis
Depends on who you talk to!
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Classification of ARF
Etiology Pre-Renal Intrinsic Renal Post-Renal
Urine Output Polyuria > 3 liters / day Oligouria: 400 – 100 cc/day Anuria: < 100 cc / day
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Urinalysis
Intrinsic Renal ARF usually has an abnormal urinalysis. Are there casts present? Is there proteinuria
present? If hematuria is present,
are the RBC’s dysmorphic?
YOU SHOULD KNOW HOW TO SPIN A PATIENT’S URINE!
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Urinalysis
Collect 10 – 20 ml of freshly voided urine in a sterile specimen container.
Take the sample to the laboratory.
Centrifuge the specimen at 2,500 rpm for 5 minutes.
Decant the supernatent.
Place the specimen on a UA microscope slide.
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Urine Microscopy
a
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Urine Microscopy, cont.
Renal Tubular Cast
Dysmorphic RBC
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Urinalysis Clinical Correlation
Nephritis: “active” urinary sediment with casts, RBC’s, WBC’s.
May be accompanied by HTN, proteinuria, ARF.
Implies inflammation and glomerular damage.
Nephrotic Syndrome: proteinuria without casts.
Proteinuria (GBM defect) Edema (low albumin) Hypoalbuminemia Lipid Abnormalities Hypercoagguable State
(AT III depletion)
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Pre-Renal ARF
Etiology Acutely reduced renal perfusion
Aortic dissection Thromboembolic disease Drugs (NSAID, ACEI)
Volume Depletion Bleeding Third Spacing Fluid Dehydration
Relative Hypotension Shock Cardiac failure (Volume depletion)
Is the patient dry? FENa < 1 %
FEUrea < 35 % BUN / Cr ratio Urine Osm and SG Urine Volume Heart Rate & BP Pulse Pressure Skin Turgor Mucous Membranes Thirst
Treatment?
Urine Na * Plasma Cr * 100
Plasma Na & Urine Cr
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NSAID’s and ACE-I in the kidneys
NSAIDInhibit PG-mediated dilatation
ACE-I inhibit arteriolar constriction
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Post-Renal ARF
Etiology of Obstruction? Foley malfunction Prostatic obstruction Neurogenic bladder Post-surgical complication Retroperitoneal fibrosis / CA Bilateral Urolithiasis
Laboratory Evaluation FENa – variable Urine Osm – variable
Radiographic Evaluation Renal US: hydonephrosis, hydroureter.
Unilateral obstruction often does not cause rise in serum creatinine (unless patient only has a single functional kidney).
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Intrinsic Renal ARF
“Active” Urine sediment implies renal involvement.
Categorized based on location of injury:
Tubules Interstitium Glomerulus Vessels
Less common systemic conditions
Pre-eclampsia TTP – HUS
Thadhani, R. et al. N Engl J Med 1996;334:1448-1460
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Acute Tubular Necrosis
Most common cause of ARF due to intra-renal causes (~ 75%)
Many causes of ATN Transient ischemic episode Toxic injury to the kidneys Myoglobinuria (Rhabdomyolysis) Heavy metals Contrast exposure
Urinalysis Iso-osmolar (300 – 400 mOsms) Urine Na > 20 FENa > 1 % “Muddy brown casts” are nonspecific,
but sensitive.
Urine Output Oligouria: more tubular damage, longer
recovery. Non-oligouria: less tubular damage,
shorter recovery time.
Still carries a high mortality.
For those who improve 90% will do so within 3 weeks 99% will do so within 6 weeks
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Microscopy of ATN
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Tubular Necrosis: Ischemia
Etiology Systemic Hypotension
Cardiogenic Shock Distributive Shock (sepsis) Hypovolemia (burns, trauma,
blood loss). Post-Surgical Anesthesia
Distributive Hypoperfusion Thyroid Storm Heart Failure ? Hepato-Renal Syndrome
Tubular cells have a high metabolism (i.e. are sensitive to states of low blood flow, hypoxia, or hypotension).
Continuum with pre-renal azotemia
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Tubular Necrosis: Nephrotoxins
Common Drugs: Amphotericin B toxicity is dependent
on the total dose (>3 gram); can also cause an RTA.
Aminoglycosides cause proximal tubule damage resulting in non-oligouric ATN.
Cisplatin is directly toxic to the tubules; also causes a magnesuria and hypomagnesemia.
Methotrexate Radiocontrast IVIG
Thadhani, R. et al. N Engl J Med 1996;334:1448-1460
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Contrast Induced Nephropathy
Radiocontrast agents Osmolality
First generation contrast agents had very high osmolality (1500 – 1800 mosm/kg)
Second generation contrast agents have lower osmolality (600 – 800 msom/kg): iohexol
Third generation agents have even lower osmolality (~290 mosm/kg): iodixanol
Ionic versus non-ionic First generation were ionic
compounds, newer products are non-ionic.
Pathogenesis is not fully understood Renal vasoconstriction? Direct toxic effect of contrast? Tubular injury from oxygen radicals?
Patient’s at highest risk Diabetes with renal insufficiency Baseline CKD (sCr > 1.5 mg/dl) High total dose of contrast (> 70 cc) Multiple Myeloma Hypovolemia (or distributive state) Concurrent Nephrotoxic Drugs
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Contrast Induced Nephropathy Prevention & Treatment
Prevention: Don’t use contrast (MRI?) Use smallest amounts possible
of non-ionic, low-osmolar contrast media.
Avoid volume depletion Avoid NSAID’s
Sodium Bicarbonate D5W + 3 amps NaHCO3/liter (~130 MEQ)
Run at 3.5 cc/kg*hour (ideal body weight) for 1 hour prior to study, and 1.2 cc/kg*hour for 6 hours after exposure
N-acetylcysteine (Mucomyst) 600 mg PO BID Administer 2 doses prior to study, and 2
doses after study.
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In Reality…
ATN is commonly multifactorial – nephrotoxic drugs exposed to kidneys with decreased perfusion
Thadhani, R. et al. N Engl J Med 1996;334:1448-1460
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Interstitial Nephritis
Acute Interstitial Nephritis Slight proteinuria +/- Renal tubular acidosis +/- Urine Eosinophils +/- RBC, WBC, and WBC Casts Caused by allergic reaction to
medication / exposure
Chronic Interstitial Nephritis Chronic analgesic abuse Heavy Meatals (lead, cadmium) Sjogren’s Disease Chronic Renal Outlet Obstruction Sickle Cell Anemia Multiple Myeloma
Antibiotic AIN Classic Triad = fever, rash, eosinophilia. Presentation is acute Common Agents
Beta-Lactams (esp Methicillin) TMP/SMX Cephalosporins Rifampin FQ
NSAID AIN Classic triad often absent Presentation subacute, or after months
of use of NSAID.
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Glomerulonephritis
First determine patient has glomerulonephritis (not just nephrotic syndrome).
If active sediment What are the serum
complement levels? Does the patient have systemic
symptoms?
Low Complement Renal Presentation
PIGN MPGN
Systemic Presentation SLE SBE Cryoglobulinemia
Normal Complement Renal Presentation
ANCA + RPGN IgA Nephropathy Alport’s Syndrome
Systemic Presentation Goodpasture’s Syndrome TTP – HUS Vasculitis
Any of the nephritic syndromes can be considered an RPGN, if it becomes rapidly progressive!
Wegener’s
PAN
Idiopathic ANCA
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Consultation…
If the patient has glomerulonephritis, you should be talking to nephrology!
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Vascular Etiology
Atheroembolic Recent intravascular
intervention Livedo reticularis Low complement Eosinophilia Blue toes
Small Vessel Disease Scleroderma TTP/HUS DIC Malignant HTN
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Acute Indications for Hemodialysis
AEIOU: Acidosis: Which is not responsive to medical therapy
Electrolytes: Hyperkalemia
Toxic Ingestion: Lithium, TCA, Ethylene Glycol, Methanol, Salicylates, (many others)
Fluid Overload: Especially in heart failure patients
Symptomatic Uremia: Bleeding, encephalopathy, pericarditis.
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What do you need to do as the Intern?
Learn about the patient’s history PMHx (CKD, CHF, Cirrhosis). Hospital Course
Recent Surgery? Contrast exposures? Hypoxic episode? Hypotensive episode? New drugs?
Labs Repeat the P2 Check a UA with micro (look at the
microscope slide yourself!) Estimate proteinuria (spot
protein/creatinine ratio)
Is the patient making urine? Post-obstruction (foley, BPH, atonic
bladder, etc) Hypovolemia or Pre-renal
Examine the Patient Vital signs Fluid status (S3, JVD, edema) Mental Status (uremia?) Bleeding (uremia? hypovolemia?) GU Exam +/- Rectal Bladder scan and/or renal US
What is the patient’s volume status?
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Intern Evaluation, cont…
What category of renal failure is present? Pre-renal Intrinsic renal Post-renal
Is there an indication for acute hemodialysis?
AEIOU
What can you do to support the patient? Fluid challenge if oligouric / anuric Remove potential nephrotoxins
Dose medications for patient’s GFR Ensure adequate renal perfusion (BP) Electrolyte management Fluid management (especially if h/o CHF,
and/or if patient is anuric!)
Remember that ARF is usually not a disease in itself, but rather the final common pathway of a variety of disease states.
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Review of ARF
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Questions?